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TCD Endocrine > Abdominal Distention and Weight Gain > Flashcards

Abdominal Distention and Weight Gain Flashcards

1
Q

Why can a pituitary tumour affect vision?

A

The optic chiasm is located directly above the sella turcica of the sphenoid bone, which contains the pituitary gland. Therefore, pituitary tumours can push/compress the optic nerve or other nerves nearby related to the extraocular muscles.

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2
Q

What signs on examination are indicative of Cushing’s Disease? (7)

A

Abdominal/truncal obesity
Abdominal striae
Neck fat (hump)
Skin bruising
High BP
Proximal myopathy
Facial plethora

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3
Q

What signs on examination are indicative of hypothyroidism? (2)

A

Bradycardia
Dry skin

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4
Q

What clinical features suggest Cushing’s Syndrome as a differential diagnosis? (2)

A

The physical findings of cushingoid appearance and presence of cardiovascular risk factors (BP, Glycosuria).

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5
Q

How can the complications of obesity be broadly classified?

A

Metabolic
Cardiorespiratory
Other

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6
Q

What is metabolic syndrome?

A

The triad of diabetes, hypertension, and obesity.

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7
Q

What BMI range is considered to be a healthy weight?

A

18.5–24.9 kg/m2

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8
Q

Which BMI ranges categorise the three classifications of obesity?

A

Obesity I: 30–34.9 kg/m2
Obesity II: 35–39.9 kg/m2
Obesity III: 40 kg/m2 or more.

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9
Q

When is medical management of obesity considered?

A

If there is a BMI of 28kg/m2 with associated risk factors, or a BMI 30kg/m2

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10
Q

What is Orlistat?

A

A pancreatic lipase inhibitor that causes reduced fat absorption.

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11
Q

What is Liraglutide (Saxenda)?

A

A GLP1 analogue that slows gastric emptying, subsequently increasing satiety

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12
Q

What are the indications for surgical management of obesity? (3)

A

-If patient has BMI > 40 or BMI 35-40 with other significant weight-related disease
-Patient has tried all non-surgical approaches
-Patient has been or is willing to receive Tier 3 weight management services

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13
Q

What four initial screening tests for Cushing’s Syndrome are used to establish underlying hypercortisolaemic state?

A

-Urinary Free Cortisol (UFC) - at least two measurements
-Late-night salivary cortisol - two measurements
-1-mg overnight Dexamethasone Suppression Test (DST)
-Longer low-dose DST (2 mg/d for 48 h)

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14
Q

What is Dexamethasone?

A

An exogeneous steroid that causes suppression of the pituitary gland through negative feedback, inhibiting ACTH secretion.

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15
Q

What is normally seen in the dexamethasone suppression test (DST)?

A

In a normal subject, there is reduction in cortisol levels following administration of low-dose dexamethasone.

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16
Q

What is seen in a patient with Cushing’s Syndrome in the dexamethasone suppression test (DST)?

A

No reduction in cortisol output after low-dose dexamethasone, but inhibition of cortisol output following high-dose dexamethasone.

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17
Q

What is seen in a patient with an adrenal tumour or ectopic ACTH in the dexamethasone suppression test (DST)?

A

No reduction in steroid production after low or high dose dexamethasone.

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18
Q

What are the main causes of ACTH-Independent Cushing’s Syndrome? (3)

A

Adrenal adenoma
Adrenal carcinoma
Adrenal hyperplasia

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19
Q

What are the main causes of ACTH-Dependent Cushing’s Syndrome? (3)

A

Pituitary adenoma
Ectopic ACTH (bronchial carcinoid commonest)
Unknown source of ACTH

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20
Q

What is the next step once hypercortisolemic state is confirmed using initial tests for Cushing’s Syndrome?

A

Arrange ACTH levels to determine ACTH Dependent CS OR ACTH-Independent CS, to help differentiate the underlying cause.

21
Q

What should be the first further investigation once ACTH-Independent Cushing’s Syndrome has been established?

A

Arrange CT Adrenals to assess adrenal tumour or hyperplasia.

22
Q

What should be the next further investigations once ACTH Dependent (pituitary dependent) Cushing’s Syndrome has been established? (2)

A

-Arrange a pituitary MRI; presence of pituitary adenoma > 6mm, is highly consistent with Cushing’s Disease.
-Arrange non-invasive tests (High-Dose Dexamethasone Suppression Test (HDDST) and Corticotropin-Releasing Hormone (CRH) stimulation test); if consistent confirms Cushing’s Disease.

23
Q

What are the consequences of removing all or part of the anterior pituitary gland? (4)

A

Hormone replacement may be needed for any of the hormones produced from the anterior pituitary gland:
-TSH (Thyroxine)
-GH (growth hormone therapy in selected few)
-ACTH (hydrocortisone therapy)
-FSH/LH (Testosterone or Oestrogen/Progesterone hormone replacement).

[The posterior pituitary hormones (ADH, Endorphins, Oxytocin) should not need replacement as they are not secreted by the pituitary gland, just stored.]

24
Q

What are pituitary tumours?

A

Benign adenomas of the anterior pituitary, broadly classified by size and the cell of origin.

25
Q

What are the five classifications of pituitary adenomas based on cell of origin?

A

Gonadotroph adenoma - mostly non-functioning
Thyrotroph adenoma - TSH producing
Corticotroph adenoma - ACTH producing (Cushing’s disease)
Lactotroph adenoma - prolactin producing
Somatotroph adenoma - GH producing (acromegaly)

26
Q

What is Metyrapone?

A

A glucocorticoid synthesis inhibitor used to reduce adrenal steroid output by inhibiting 11-beta-hydroxylase.

27
Q

What are the hormonal consequences of removing both adrenal glands?

A

Glucocorticoid and mineralocorticoid hormone deficiencies, requiring replacement therapy.

28
Q

What immediate action should be taken if you suspect established or developing adrenal crisis in a patient?

A

Immediate injection of 100mg hydrocortisone i.v. or i.m., followed by rapid rehydration with i.v. administration of 0.9% saline solution (or equivalent).

29
Q

What are the ‘sick day rules’ with regards to glucocorticoid replacement therapy?

A

The patient should double the dose of their glucocorticoids in the event of any medical illness; physical and mental stress; and trauma including any surgical procedure.

30
Q

What are the three types of adrenal insufficiency?

A

-Primary (due to adrenocortical disease – adrenal glands are not able to respond to ACTH)
-Secondary (pituitary dysfunction – lack of ACTH needed to stimulate the adrenal glands)
-Tertiary (hypothalamus – lack of corticotrophic releasing hormone [CRH])

31
Q

Why are secondary and tertiary adrenal insufficiency associated with cortisol but not mineralocorticoid deficiency?

A

Aldosterone (mineralocorticoid) is primarily regulated by renin-angiotensin system, which is independent of pituitary and hypothalamus action.

32
Q

What does NICE Guidance suggest if serum cortisol is below 100nmol/l?

A

Admit patient to hospital, as adrenal insufficiency is highly likely. Urgency depends on severity of symptoms and serum cortisol level.
(Postural hypotension and/or electrolyte disturbance are indications for urgent referral or admission.)

33
Q

What is the Short Synacthen Test (aka Short ACTH stimulation test)?

A

A test that assesses adrenocortical functional activity in response to the injection of exogenous ACTH (tetracosactrin).
—>Cortisol levels fail to increase in response to exogenous ACTH in patients with chronic adrenal insufficiency.

34
Q

What main signs are highly indicative of Addison’s Disease? (3)

A

Hyperpigmentation - only seen in Addison’s, due to elevated levels of ACTH.
Electrolyte disturbance and significant postural hypotension - due to lack of mineralocorticoids causing hypovolaemia and sodium loss, hence commonly noticed in Addison’s Disease.

35
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

Cushing’s Syndrome - a syndrome characterised by excess glucocorticoids from any cause.
Cushing’s Disease - pituitary dependent Cushing’s Syndrome (due to a pituitary ACTH producing adenoma)

36
Q

What is corticotropin-releasing hormone (CRH)?

A

A hypothalamic peptide, which acts on pituitary corticotrophs to stimulate secretion of ACTH.

37
Q

What features are always indicative of Adrenal Crisis? (3)

A

A sick patient with hypotension and hyponatraemia.

38
Q

What is Adrenal Insufficiency?

A

Adrenal insufficiency is primarily inadequate secretion of cortisol and/or aldosterone to maintain normal physiological function.

39
Q

What main symptoms are highly indicative of Addison’s Disease? (5)

A

Weakness
Weight loss
Severe fatigue
Loss of appetite
Dizziness and blackouts

[WWSLD]

40
Q

How is Addison’s Disease managed? (2)

A

The individual takes replacement steroids, titrated to severity of disease: hydrocortisone (a glucocorticoid) replaces cortisol and fludrocortisone (a mineralocorticoid) can replace aldosterone if this is also insufficient.

41
Q

How is a diagnosis of Chronic Adrenal Insufficiency confirmed?

A

A short ACTH (Synacthen) Stimulation Test, followed by subsequent investigations to explore underlying cause.

42
Q

What is the difference between adrenal insufficiency and Addison’s Crisis?

A

Adrenal insufficiency is chronic and presents insidiously with non-specific symptoms; Addisonian Crisis (or acute adrenal crisis) is an acute crisis in patients with existing adrenal insufficiency.

43
Q

Which region of the adrenal gland is Cushing’s Syndrome related to?

A

The zona fasiculata.

44
Q

What substance are hormones produced by the adrenal glands synthesised from?

A

Cholesterol

45
Q

What additional investigation can help determine the cause of hyponatraemia?

A

Blood volume - if patient is euvolaemic, hypovolaemic or hypervolaemic.

46
Q

What are the potential causes of hyponatraemia in a hypervolaemic patient? (4)

A

Heart failure
Nephrotic syndrome
Cirrhosis
Chronic kidney disease

47
Q

What is the first indicator of diabetic nephropathy?

A

Microalbuminuria

48
Q

Briefly describe the HPA axis for glucocorticoid release.

A

Hypothalamus releases corticotropin releasing factor (CRF) which stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to release cortisol, corticosterone and other exogenous steroids.

TCD Endocrine (5 decks)

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